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Embolic disorders

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thrombo-embolic disorders, e g. pulmonary embolism, deep-vein thrombosis and arterial occlusiorrs. It is also used in acute myocardial irtfarclioa... [Pg.475]

Streptokinase is a widely employed thrombolytic agent. It is administered to treat a variety of thrombo-embolic disorders, including ... [Pg.350]

Higher molecular mass dextrans (partieularly dextran 70, 75 and 110) are used to promote short-term expansion of plasma volume thus preventing/treating shoek due to blood loss. A 6% w/v solution of these dextrans exerts an osmotie pressure similar to that of plasma proteins. Generally, an initial dose of 500 ml 1 litre is administered by i.v. infusion. Dextrans also inhibit the aggregation of red blood eells. Thus, they are often used to prevent/treat post-operative thrombo-embolic disorders (see later in this ehapter) and to improve blood flow. [Pg.355]

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. [Pg.134]

Cause Most common is cerebrovascular occlusion. Other causes include intracranial hemorrhage, cardiac embolisms, infection, and clotting disorders. [Pg.1007]

Pulmonary embolism A disorder of thrombus formation causing obstruction of a pulmonary artery or one of its branches may result in pulmonary infarction. [Pg.1575]

Thrombotic disorders Thrombotic disorders (thrombophlebitis, cerebrovascular disorders, retinal thrombosis, pulmonary embolism) occasionally occur in patients taking progestins. [Pg.195]

Fever is common in, and often a sign of, infection irrespective of its cause. Other diseases, which cause fever, are tumours, non-infectious inflammations, endocrine disorders and thrombo-embolic disease. Drugs can cause fever, e.g. angiotension-II-antagonists, ACE inhibitors and phenytoin. [Pg.499]

The most prescribed drugs for blood-related disorders are also summarized in Table 1.17. Blood clots can occur in the veins at extremities (especially after a long period of immobility). Those clots can subsequently become lodged in the blood vessels, the atria, the heart valves, and within the lungs, causing embolism and shortness of breath. Under severe conditions, the clots can also obstruct the flow of blood to the brain, leading to a stroke and paralysis. Coumadin (warfarin see chemical structure below) is one of the main hematological compounds that has been widely prescribed to counter these conditions... [Pg.74]

Pleural effusion, pulmonary embolism, bone fracture, thromboembolic disorder,... [Pg.680]

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. [Pg.17]

Calcification, and possibly sclerosis, of the aortic and mitral valves may be a cause of embolism of calcific or complicating thrombotic material. However, these degenerative disorders of heart valves are so common, particularly in the elderly, that it has been very difficult to associate them causally with stroke (Boon et al. 1996). [Pg.65]

Thrombophilias and other causes of hypercoagulability are rare causes of stroke (Matijevic and Wu 2006). Antithrombin III deficiency, protein C deficiency, activated protein C resistance owing to factor V Leiden mutation, protein S deficiency and plasminogen abnormality or deficiency can all cause peripheral and intracranial venous thrombosis. Thrombosis is usually recurrent and there is often a family history. Thrombophilia may cause arterial thrombosis, although the alternative diagnosis of paradoxical embolism should always be considered in patients with these disorders. It should be noted that deficiencies in any one of the factors associated with thrombophilia may be an incidental finding and cannot necessarily be assumed to be the cause of stroke. [Pg.75]

Fibrocartilaginous embolism is a rare and curious disorder where fibrocartilaginous emboli, presumably from degenerative intervertebral disc material, are found in various organs, the spinal cord more often than the brain (Freyaldenhoven et al. 2001). [Pg.81]

Bathen J, Sparr S, Rokseth R (1978). Embolism in sinoatrial disease. Acta Medica Scandinavica 203 7-11 Berkovic SF, Bladin PF, Darby DG (1984). Metabolic disorders presenting as stroke. Medical Journal of Australia 140 421-424... [Pg.82]

Schmahmann JD (2003). Vascular syndromes of the thalamus. Stroke 34 2264-2278 Schulz UG, Rothwell PM (2001). Major variation in carotid bifurcation anatomy a possible risk factor for plaque development Stroke 32 2522-2529 Scott BL, Jankovic J (1996). Delayed-onset progressive movement disorders after static brain lesions. Neurology 46 68-74 Wardlaw JM, Merrick MV, Ferrington CM et al. (1996). Comparison of a simple isotope method of predicting likely middle cerebral artery occlusion with transcranial Doppler ultrasound in acute ischaemic stroke. Cerebrovascular Diseases 6 32-39 Wardlaw JM, Lewsi SC, Dennis MS etal. (1999). Is it reasonable to assume a particular embolic source from the type of stroke Cerebrovascular Diseases 9(Supp 1) 14... [Pg.131]


See other pages where Embolic disorders is mentioned: [Pg.17]    [Pg.17]    [Pg.137]    [Pg.682]    [Pg.129]    [Pg.910]    [Pg.387]    [Pg.347]    [Pg.956]    [Pg.1]    [Pg.17]    [Pg.128]    [Pg.296]    [Pg.216]    [Pg.218]    [Pg.236]    [Pg.289]    [Pg.188]    [Pg.178]    [Pg.60]    [Pg.63]    [Pg.70]    [Pg.309]    [Pg.288]    [Pg.183]    [Pg.288]    [Pg.1563]    [Pg.2439]   
See also in sourсe #XX -- [ Pg.17 ]




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